Pressure ulcer development and vasopressor agents in adult critical care patients: a literature review.

Critical care units provide technologically sophisticated care to the sickest patients in the healthcare system. The contribution of iatrogenic factors, including administration of pharmacologic agents such as vasopressors, to pressure ulcer (PU) development in adult critical care patients is understudied, thus less understood, but may be an important PU risk factor to consider in the critical care population. Vasopressor agents are potent vasoconstrictors commonly administered to critical care patients to elevate mean arterial pressure to counteract the effects of inadequate tissue perfusion and hypoxia; they have reemerged over the past decade in contemporary intensive care units as important first-line drugs in the treatment of shock states. A comprehensive review of the literature was undertaken in order to determine the level of evidence regarding the relationship between vasopressor agents (norepinephrine, epinephrine, phenylephrine, vasopressin, and dopamine) and PU development in adult critical care patients. Computerized databases of EBSCOCINAHL and OVID MEDLINE were searched for English-language publications from 2000 to the present using the following terms: pressure ulcer, vasopressor, norepinephrine, epinephrine, vasopressin, dopamine, phenylephrine, critical care and pressure ulcers; intensive care and pressure ulcers; and pressure ulcer risk factors. Ten studies were identified that met the inclusion/exclusion criteria. Statistically significant associations were reported between the broad category of vasopressor agents and PU development in seven studies. Of those, two identified a specific vasopressor agent (norepinephrine) as a significant predictor of PU development in this population. Empirical support for the broad category of vasopressors as a PU risk factor is increasing, and a small body of evidence is emerging to support the role of one specific vasopressor (norepinephrine) in PU development. Increased vigilance regarding PU risk in critical care patients receiving vasopressor agents may be warranted. However, studies are needed to examine the effects of individual vasopressor agents and dosage and duration thresholds, as well as empirical investigation regarding the synergistic effect of multiple vasopressor agents administered simultaneously, on PU development in this population. Finally, research is needed to further elucidate vasopressor use as an independent risk factor for PU development in this population.